![]() There are still many outstanding questions that need to be explored. However, the specific mechanisms of abnormally expressed lncRNAs in cancer cells remain unclear. Numerous lncRNAs are abnormally expressed in specific cancer types ( 22) and participate in a variety of complex biological processes by interacting with proteins, DNA, as well as RNAs ( 23– 26). Interestingly, the number of lncRNAs far exceeds the number of protein-coding genes ( 21). Based on the chromosomal position of the lncRNAs, they are divided into antisense lncRNAs, intronic lncRNAs, divergent lncRNAs, intergenic lncRNAs, promoter-associated lncRNAs, transcription start site-associated lncRNAs, and enhancer RNAs (eRNAs) ( 16– 20). LncRNAs are structurally similar to mRNAs and are also generated through DNA transcription ( 15). These studies highlight the essential role of lncRNAs in cancer development and progression, as well as their potential as novel therapeutic targets for multiple tumors. Previous studies showed that lncRNAs are involved in the regulation of cell survival, growth ( 6– 10), invasion, and metastasis ( 11), maintenance of stemness ( 12, 13), as well as tumor angiogenesis ( 14). LncRNAs were originally thought to be by-products transcribed by RNA polymerase II and have no biological function however, with the development of high-throughput sequencing technology, an increasing number of lncRNAs have been annotated, and their functions of lncRNAs in tumorigenesiss and tumor progression have been gradually elucidated. LncRNAs are a class of RNA molecules comprised of more than 200 nucleotides, which do not encode proteins. Many regulatory RNAs harboring various sizes have been discovered ( 4), especially long non-coding RNAs (lncRNAs) ( 5). In 1961, the central position of RNA in the flow of genetic information was revealed ( 1) and in the following 50 years, the emergence of whole-genome sequencing technology has greatly accelerated our understanding of both coding and non-coding RNAs (ncRNAs) ( 2, 3). Therefore, it is of paramount importance to understand the underlying mechanism through which non-coding genes influence the tumorigenic process. With the widespread application of next-generation sequencing (NGS) technology, a large number of non-coding genes have been identified and found to be strongly associated with tumor development and progression. While cancer awareness is gradually increasing worldwide, the current focus is still concentrated on the DNA sequence responsible for the abnormal protein synthesis. Over the past few decades, oncogenes such as Src and Ras have been discovered, and the functions of their encoded proteins have been elucidated. This review will provide a short but comprehensive description of the lncRNA functions in tumor development and progression, thus accelerating the clinical implementation of lncRNAs as tumor biomarkers and therapeutic targets.Ĭancer is a complex disease associated with multiple genetic mutations. Additionally, we summarize the research strategies used to investigate the roles of lncRNAs in tumors, including lncRNAs screening, lncRNAs characteristic analyses, functional studies, and molecular mechanisms of lncRNAs. We focused on the signal, decoy, guide, and scaffold functions of lncRNAs at the epigenetic, transcription, and post-transcription levels in cancer cells. Here, we discuss the recent advances in understanding of the specific regulatory mechanisms of lncRNAs. Furthermore, lncRNAs and the pathways they influence might represent promising therapeutic targets for a number of tumors. Increasing evidence indicates that lncRNAs exert an irreplaceable role in tumor initiation, progression, as well as metastasis, and are novel molecular biomarkers for diagnosis and prognosis of cancer patients. LncRNAs are more than 200 nucleotides in length and lack protein-coding potential. ![]() The development and application of whole genome sequencing technology has greatly broadened our horizons on the capabilities of long non-coding RNAs (lncRNAs). 4Laboratory for Cell Biology, College of Life Sciences of Zhengzhou University, Zhengzhou, China.3Faculty of Medicine, St George and Sutherland Clinical School, St George Hospital, The University of New South Wales (UNSW) Sydney, Kensington, NSW, Australia.2Translational Medicine Research Center, People’s Hospital of Zhengzhou, Zhengzhou, China.1Department of Pharmacology, School of Basic Medicine, Zhengzhou University, Zhengzhou, China.Na Gao 1, Yueheng Li 1, Jing Li 1, Zhengfan Gao 1, Zhenzhen Yang 1,2, Yong Li 1,3, Hongtao Liu 4* and Tianli Fan 1* ![]()
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